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To assess the value of Presepsin and Pentraxin3 measurement in critically ill children.Prospective observational study conducted on 80 children admitted into Pediatric Intensive Care Unit (PICU) and 80 healthy controls. Patients were evaluated for presence of sepsis. Pediatric Risk of Mortality (PRISM) and Pediatric Index of Mortality (PIM2) were calculated. Serum Presepsin and Pentraxin3 were measured within 24 h of admission.Presepsin and Pentraxin3 were significantly higher among the whole patient cohort and among septic patients compared with controls (p 0.001) but no difference was found between septic and non-septic patients. Pentraxin3, but not Presepsin, was significantly higher among non-survivors compared with survivors (p = 0.048) and was correlated with PIM2. Receiver operating characteristic (ROC) curve analysis revealed that Pentraxin3 had an AUC of 0.631 for prediction of mortality which was comparable to that of PRISM and PIM2. Presepsin was associated with a higher rate of mechanical ventilation and longer PICU stay.Presepsin and Pentraxin3 are acute phase proteins potentially useful for monitoring critically ill children and diagnosing sepsis. Pentraxin3 is associated with mortality but modestly discriminates survivors from non-survivors. Presepsin is associated with certain indicators of disease severity. Larger studies are certainly required.

BackgroundMean platelet volume (MPV), may help to determine atherosclerosis threat. Cardiovascular disease is one of the common causes of morbidity and mortality in patients having psoriasis.ObjectiveTo examine MPV as a biomarker for subclinical atherosclerosis in psoriasis patients, compared with i

Aim: To estimate the blood level of Erythropoietin(EPO) in neonates with anemia of prematurity (APO) and in late hypo-regenerative anemia and to clarify role of EPO in correction of anemia and reducing the number of blood transfusions. Methods: This study was carried out on 60 neonates divided into; group I (30 preterm neonates) with AOP received EPO (250 IU/kg/dose subcutaneously 3 times weekly for 4 weeks), compared to group II (30 neonates) with AOP treated only with blood transfusion. CBC parameters and transfusion requirements were followed during therapy. Serum level of EPO was measured by ELISA technique. Results: By the end of the 4th week of therapy, there was significant increase in group I post r-Hu EPO compared to group II regarding reticulocyte counts (P

Purpose Despite the advances in the pharmacological treatment of epilepsy, pharmacoresistance still remains challenging. Understanding of the pharmacogenetic causes is critical to predict drug response hence providing a basis for personalized medications. Genetic alteration in activity of drug target and drug metabolizing proteins could explain the development of pharmacoresistant epilepsy. So the aim of this study was to explore whether SCN1A c. 3 184 A/G (rs2298771) and CYP3A5*3 (rs776746) polymorphisms could serve as genetic based biomarkers to predict pharmacoresistance among Egyptian epileptic children. Methods Genotyping of SCN1A c.3184 A/G and CYP3A5*3 polymorphisms using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method was performed in 65 healthy control subjects and 130 patients with epilepsy, of whom 50 were drug resistant and 80 were drug responsive. Results There was a significant higher frequency of the AG genotype ( p =0.001) and G allele ( p =0.006) of SCN1A polymorphism in epileptic patients than in controls. Also their frequency was significantly higher in drug resistant patients in comparison with drug responders ( p =0.005 and 0.054 respectively). No significant association between CYP3A5*3 polymorphism and drug-resistance was found. Conclusions Overall, results confirmed the claimed role of SCN1A c.3184 A/G polymorphism in epilepsy and moreover in development of pharmacoresistance among Egyptian epileptic children. CYP3A5*3 variants have no contributing effect on pharmacoresistance among Egyptian epileptic children.

Despite progress in terms of management, breast cancer still constitutes a major threat to health worldwide. Various microRNAs have been shown to play a fundamental role in tumor biology during development and progression. Therefore, our study was focused on investigating the role of circulating microRNA122 (miR-122) in breast cancer and its clinical utility as a potential easily accessible biomarker for use in the diagnostic and prognostic assessment of breast cancer. Determination of the serum CA15-3 and carcinoembryonic antigen levels was conducted using an enzyme-linked immunosorbent assay. The expression level of miR-122 was determined using real time PCR in 90 breast cancer patients and 60 healthy controls. Higher circulating miR-122 levels were found in breast cancer patients than in controls and higher miR-122 levels were observed in patients who experienced metastasis. Additionally, miR-122, at a cutoff > 2.2, had a sensitivity of 93.33% and a specificity of 90% when used to distinguish breast cancer patients from controls and was able to predict metastasis at a cutoff > 10.9 with a sensitivity of 95.83% and a specificity of 65.15%. Kaplan–Meier survival analysis revealed that high miR-122 expression is significantly associated with decreased overall survival and progression-free survival. This study concludes that circulatory miR-122 could be utilized as a diagnostic and prognostic biomarker in breast cancer patients.

Objective The aim of this study was to measure serum leptin levels in children with cyanotic and acyanotic congenital heart disease and to examine its possible role in growth in these children. Background Leptin has been shown to be an integral component of energy homeostasis and regulation of body weight. Leptin regulates adipose tissue mass and correlates with the fat mass. Research on the physiological function of leptin has primarily focused on its role in the pathogenesis of obesity. Children with congenital heart disease are at increased risk for poor growth. Several factors may play a role in poor growth, including feeding difficulties, increased caloric requirements, and the effects of cardiac lesions on growth regulation. Patients and methods This study was carried out over 1 year on 35 patients with congenital heart disease [20 patients were acyanotic (12 boys, 8 girls) and 15 patients were cyanotic (9 boys, 6 girls)] in the Pediatric Cardiology Department in Menoufia University Hospital and 35 apparently healthy children of the same age (range: 3 months–12 years), sex, and socioeconomic status. All patients and controls were subjected to a complete assessment of history, a thorough clinical examination, chest radiograph, ECG, echocardiography, and measurement of serum leptin level. Results Children with cyanotic congenital heart disease had statistically significant lower weight, length, mid-arm circumference, and BMI. There was no statistically significant difference in serum leptin levels in the cyanotic, acyanotic, and control groups. Serum leptin level was correlated positively with BMI and mid-arm circumference in all groups. Conclusion Serum leptin level did not change in children with acyanotic and cyanotic congenital heart disease, suggesting that other factors may regulate nutrient intake, growth, weight, and energy input and output in these children.

Idiopathic nephrotic syndrome (INS) is a glomerular disease with completely unclear pathogenesis and different responses to steroid therapy. This study aimed to investigate the role of cytokine genes promoter polymorphisms in steroid therapy responses.One hundred children with INS and 30 healthy controls were studied. Genotyping of TNF-α-G308A single nucleotide polymorphism was done using polymerase chain reaction-restriction fragment length polymorphism method, while of IL-6-G174C single nucleotide polymorphism was done using real-time polymerase chain reaction.The IL-6-G174C exhibited a significantly different genotype distribution among the children with INS compared with the controls (GG versus CC, P = .02; GG versus GC, P = .003; odds ratio [OR], 5.83; 95% confidence interval [CI], 1.64 to 20.70; as well as alleles distribution of G versus C, P ? .001; OR, 7.57; 95% CI, 2.28 to 25.17). With regard to TNF-α-G308A genotype, there was no significant difference in genotype distribution of the children with INS compared with the controls, but a significant difference was observed at the alleles level. Comparing the steroid-resistant group with the steroid-sensitive group, significant association was found at genotypic level in case of IL-6-G174C (GG versus CC, P = .03; OR, 5.52; 95% CI, 1.39 to 21.89), but no association was found regarding GG versus GC. At the allelic level of IL-6-G174C, there was no significant association either.IL-6-G174C and TNFα-G308A polymorphisms may affect susceptibility to idiopathic nephrotic syndrome and might affect steroid response in INS patients.

This study evaluated the association of NOS3 polymorphisms with hypertension risk and complications. eNOS (G894T) SNP was performed by RT-PCR on 70 hypertensive patients (25 were hypertensive, 25 were hypertensive with CAD, and 20 were diabetic with hypertension) and 30 age- and gender-matched individuals. Lipid and glucose profile were assessed by standard colorimetric assay. Our results revealed that combination of (GT + TT) genotype and T allele significantly increases the risk of hypertension (OR = 3.86 and 4.33), respectively. Subgroup analysis showed significant association between CAD with eNOS (G894T) mutant genotype (P = 0.002) and allele frequency (P

Objectives This study aimed to study the role of allergy diagnosed by immunoglobulin E (IgE) in the etiology of pediatric otitis media with effusion (OME) by detection of IgE in middle-ear effusion using the enzyme-linked immunosorbent assay technique. Background The role of allergy in chronic OME is controversial. Patients and methods This was a prospective study that was carried out on 80 cases; including 60 pediatric patients diagnosed with chronic OME [resistant to medical treatment for >3 months (type B tympanogram) or recurrent after successful medical treatment]. Patients were subjected to a myringotomy with insertion of a tympanostomy tube (grommet tube). Their age ranged from 2 to 15 years. Twenty children had ENT disease other than OME, mostly adenoidal or tonsillar hypertrophy. The serum level of total IgE was assayed in patients and control groups as well as in the middle-ear effusion of patients. Results The results showed that total IgE was higher in the serum of patients with OME than the serum of the control group; there was a high significant correlation between total IgE in serum and total IgE in effusion in patients with OME. Conclusion Allergy is a possible risk factor for the development of pediatric OME.

Background/Aim: There is no doubt that colorectal cancer (CRC) poses a major threat to public health worldwide, and despite improvement in managements, prognosis still remains an irritating question with no definite answer. Being a fundamental player in cancer metabolism, glucose transporter 1 (GLUT1) could be utilized as a prognostic biomarker that could fuel development of new treatment strategies. The aim of this study was to assess the validity of GLUT1 expression as a prognostic biomarker and to elucidate to what extent it is immersed in poor clinical outcome among CRC patients. Patients and Methods: GLUT1 expression in peripheral blood specimens was analyzed by quantitative real-time polymerase chain reaction in 47 CRC patients and 20 healthy controls. Results: There was significantly elevated GLUT1 expression in peripheral blood of CRC patients than in controls (P < 0.001). The cutoff value of 0.605 provided 98% sensitivity and 100% specificity. There were significantly higher values of GLUT1 expression in patients under 50 years (P = 0.003), performance status 2 (P = 0.009), stage IV (P < 0.001), and presence of metastasis (P < 0.001). GLUT1 expression showed nonsignificant association with overall survival (P = 0.068), while tumor stage (P = 0.01) and metastasis (P = 0.009) were significantly associated with lower overall survival. Conclusion: GLUT1 is sensitive and specific marker for CRC. It is overexpressed in young age patients, poor performance status, and stage IV patients. Although this was not statistically significant, GLUT 1 showed higher expression level in patients with lesser survival.

Objective The aim of the study was to assess the association between heat shock protein (HSP) 70-2 + 1267 A/G polymorphism and diabetic nephropathy (DN) in type II diabetes mellitus. Background DN is a life-threatening microvascular complication of type II diabetes. Oxidative stress plays a main role in its pathogenesis. As a consequence, a cellular adaptive response occurs requiring functional chaperones, so that the induction of HSPs is a maintained response in counteracting this oxidative stress. HSP70-2 + 1267 A/G and HSP70-hom + 2437 T/C polymorphisms may play an important role in susceptibility to and/or progression of DN. Patients and methods Sixty type II diabetic patients (30 patients with DN and 30 patients free of DN) and 20 healthy individuals, as the control group, were selected. Participants were genotyped for the HSP70-2 + 1267 A/G and HSP70-hom + 2437 T/C polymorphisms by PCR/restriction fragment length polymorphism. Results There was significant difference for HSP70 - 2 + 1267 A/G polymorphism. GG genotype and G allele were more frequent in the DN group versus other groups, whereas there was no significant difference in genotype and allele distributions among the three studied groups for the HSP70-hom polymorphism. On comparing diabetics with nephropathy versus diabetics without nephropathy, the odds ratio of the risk allele (G) of HSP70 - 2 + 1267 was 4.60 (95% confidence interval 2.09-10.12) and was 0.45 (95% confidence interval 0.15-1.42) for the risk allele (C) of HSP70-hom + 2437 T/C polymorphism. Conclusion HSP70 - 2 + 1267 A/G polymorphism is associated with renal complications in type II diabetic patients and may be useful in identifying patients with increased risk for DN.